Effects of matrine, artemisinin, and tetrandrine [Ca2+](i) in guinea pig ventricular myocytes

AIM: To compare the effects of matrine, artemisinin, and tetrandrine on int racellular Ca2+ concentration ([Ca2+](i)) in guinea pig ventricular myocyte s. METHODS: A single ventricular myocyte was loaded with Fluo 3-acetoxymeth yl (Fluo 3-AM). [Ca2+](i) was recorded by laser scanning confocal microscop e and represented by fluorescence intensity (m). RESULTS: 1) KCl 60 mmol .L -1 elevated the FI from 299 +/- 19 to 1389 +/- 325 (P <0.01) in the presenc e of extracellular Ca2+ 1.8 mmol L-1. 2) Both matrine and artemisinin at th e concentration of 100 mu mol .L-1 could enhance the increase of FI by KCl 60 mmol .L-1. The FI values reached 1495 +/- 320 and 1646 +/- 308 from 301 +/- 14 and 299 +/- 16 (P < 0.01), respectively. 3) Both tetrandrine 1, 10, and 100 mu mol .L-1 and verapamil 10 mu mol .L-1 inhibited the influx of ex tracellular Ca2+ induced by KCl 60 mmol .L-1. 4) Matrine 1, 10, and 100 mu mol .L-1 could elevate the FI in the presence of extracellular Ca2+. The FI values reached 441 +/- 96, 504 +/- 112, and 643 +/- 126 from 303 +/- 27, 3 00 +/- 32, and 296 +/- 19 (P < 0.05), respectively. 5) Tetrandrine 1 and 10 mu mol .L-1 could apparently inhibited Ca2+ release from intracellular cal cium stores induced by caffeine 20 mmol .L-1 (P < 0.05). CONCLUSION: Effect s of matrine, artemisinin, and tetrandrine on [Ca2+](i) in ventricular myoc ytes were different. Both artemisinin and matrine could enhance Ca2+ entry induced by KCl, while tetrandrine, as verapamil did, inhibited this kind of Ca2+ entry. Matrine itself could produce Ca2+ entry.